Changes in the diet of hake associated with El Niño 1997?1998 in the northern Humboldt Current ecosystem

International audienceHake (Merluccius gayi peruanus) predation plays an important role in the dynamics of the Humboldt Current ecosystem (HCE). Changes in the hake trophic habits associated with physical variability are expected to impact prey populations and to propagate through the food web. Time series (1995?2002) of (a) stomach contents of hake, (b) biomass estimations of fish prey species of hake, and (c) depth of the 15°C isotherm was analysed with the aim of exploring the impacts of El Niño 1997?1998 on the diet of hake. Biomass estimations of fish prey species were used to indicate resource availability, and depth of the 15°C isotherm to represent variability associated with the ENSO cycle in the physical environment of hake. The richness of prey species increased during the months when 15°C isotherm reached its deepest position, supporting the hypothesis of increased biodiversity (tropicalization) of the HCE during El Niño events. An increased variability in stomach fullness of hake was detected after 1999 which could indicate high heterogeneity in the food supply as a consequence of impacts of the warm event in the biotic community structure of the HCE, a physiological impairment of hake or an effect of the abrupt reduction in the mean total length of hake, postulated as a compensatory response to fishery pressure. Hake can be characterized as an opportunist predator according to the observed changes in its diet during 1995?2002. Overall, the diet of hake in the northern HCE exhibited transitory (e.g. increased richness of prey species in the stomach contents) and medium term (e.g. increased variability in feeding activity) responses associated with El Niño 1997?1998, which should be incorporated both in population dynamics and food web analyses

Measurements and modelling of stray magnetic fields and the simulation of their impact on the Compact Linear Collider at 380 GeV

The Compact Linear Collider (CLIC) targets a nanometre beam size at the collision point. Realising this beam size requires the generation and transport of ultra-low emittance beams. Dynamic imperfections can deflect the colliding beams, leading to a collision with a relative offset. They can also degrade the emittance of each beam. Both of these effects can significantly impact the luminosity of CLIC. In this paper, we examine a newly considered dynamic imperfection: stray magnetic fields. Measurements of stray magnetic fields in the Large Hadron Collider tunnel are presented and used to develop a statistical model that can be used to realistically generate stray magnetic fields in simulations. The model is used in integrated simulations of CLIC at 380GeV including mitigation systems for stray magnetic fields to evaluate their impact on luminosity

Measurements of sub-nT dynamic magnetic field shielding with soft iron and mu-metal for use in linear colliders

There is an increasing need to shield beams and accelerator elements from stray magnetic fields. The application of magnetic shielding in linear colliders is discussed. The shielding performance of soft iron and mu-metal is measured for magnetic fields of varying amplitude and frequency. Special attention is given to characterise the shielding performance for very small-amplitude magnetic fields

Design and operation of a prototype interaction point beam collision feedback system for the International Linear Collider

A high-resolution, intratrain position feedback system has been developed to achieve and maintain collisions at the proposed future electron-positron International Linear Collider (ILC). A prototype has been commissioned and tested with a beam in the extraction line of the Accelerator Test Facility at the High Energy Accelerator Research Organization in Japan. It consists of a stripline beam position monitor (BPM) with analogue signal-processing electronics, a custom digital board to perform the feedback calculation, and a stripline kicker driven by a high-current amplifier. The closed-loop feedback latency is 148 ns. For a three-bunch train with 154 ns bunch spacing, the feedback system has been used to stabilize the third bunch to 450 nm. The kicker response is linear, and the feedback performance is maintained, over a correction range of over $\pm$60 {\mu}m. The propagation of the correction has been confirmed by using an independent stripline BPM located downstream of the feedback system. The system has been demonstrated to meet the BPM resolution, beam kick, and latency requirements for the ILC

Natural history of murine gamma-herpesvirus infection

Murine gamma-herpesvirus 68 (MHV-68) is a natural pathogen of small rodents and insectivores (mice, voles and shrews). The primary infection is characterized by virus replication in lung epithelial cells and the establishment of a latent infection in B lymphocytes. The virus is also observed to persist in lung epithelial cells, dendritic cells and macrophages. Splenomegaly is observed two weeks after infection, in which there is a CD4+ T-cell-mediated expansion of B and T cells in the spleen. At three weeks post-infection an infectious mononucleosis-like syndrome is observed involving a major expansion of Vbeta4+CD8+ T cells. Later in the course of persistent infection, ca. 10% of mice develop lymphoproliferative disease characterized as lymphomas of B-cell origin. The genome from MHV-68 strain g2.4 has been sequenced and contains ca. 73 genes, the majority of which are collinear and homologous to other gamma-herpesviruses. The genome includes cellular homologues for a complement-regulatory protein, Bcl-2, cyclin D and interleukin-8 receptor and a set of novel genes M1 to M4. The function of these genes in the context of latent infections, evasion of immune responses and virus-mediated pathologies is discussed. Both innate and adaptive immune responses play an active role in limiting virus infection. The absence of type I interferon (IFN) results in a lethal MHV-68 infection, emphasizing the central role of these cytokines at the initial stages of infection. In contrast, type II IFN is not essential for the recovery from infection in the lung, but a failure of type II IFN receptor signalling results in the atrophy of lymphoid tissue associated with virus persistence. Splenic atrophy appears to be the result of immunopathology, since in the absence of CD8+ T cells no pathology occurs. CD8+ T cells play a major role in recovery from the primary infection, and also in regulating latently infected cells expressing the M2 gene product. CD4+ T cells have a key role in surveillance against virus recurrences in the lung, in part mediated through 'help' in the genesis of neutralizing antibodies. In the absence of CD4+ T cells, virus-specific CD8+ T cells are able to control the primary infection in the respiratory tract, yet surprisingly the memory CD8+ T cells generated are unable to inhibit virus recurrences in the lung. This could be explained in part by the observations that this virus can downregulate major histocompatibility complex class I expression and also restrict inflammatory cell responses by producing a chemokine-binding protein (M3 gene product). MHV-68 provides an excellent model to explore methods for controlling gamma-herpesvirus infection through vaccination and chemotherapy. Vaccination with gp150 (a homologue of gp350 of Epstein-Barr virus) results in a reduction in splenomegaly and virus latency but does not block replication in the lung, nor the establishment of a latent infection. Even when lung virus infection is greatly reduced following the action of CD8+ T cells, induced via a prime-boost vaccination strategy, a latent infection is established. Potent antiviral compounds such as the nucleoside analogue 2'deoxy-5-ethyl-beta-4'-thiouridine, which disrupts virus replication in vivo, cannot inhibit the establishment of a latent infection. Clearly, devising strategies to interrupt the establishment of latent virus infections may well prove impossible with existing methods

In vivo imaging of murid herpesvirus-4 infection

Luciferase-based imaging allows a global view of microbial pathogenesis. We applied this technique to gammaherpesvirus infection by inserting a luciferase expression cassette into the genome of murine herpesvirus-4 (MuHV-4). The recombinant virus strongly expressed luciferase in lytically infected cells without significant attenuation. We used it to compare different routes of virus inoculation. After intranasal infection of anaesthetized mice, luciferase was expressed in the nose and lungs for 7–10 days and in lymphoid tissue, most consistently the superficial cervical lymph nodes, for up to 30 days. Gastrointestinal infection was not observed. Intraperitoneal infection was very different to intranasal, with strong luciferase expression in the liver, kidneys, intestines, reproductive tract and spleen, but none in the nose or lungs. The nose has not previously been identified as a site of MuHV-4 infection. After intranasal infection of non-anaesthetized mice, it was the only site of non-lymphoid luciferase expression. Nevertheless, lymphoid colonization and persistence were still established, even at low inoculation doses. In contrast, virus delivered orally was very poorly infectious. Inoculation route therefore had a major impact on pathogenesis. Low dose intranasal infection without anaesthesia seems most likely to mimic natural transmission, and may therefore be particularly informative about normal viral gene functions

Nonrandom Distribution of Vector Ticks (Dermacentor variabilis) Infected by Francisella tularensis

The island of Martha's Vineyard, Massachusetts, is the site of a sustained outbreak of tularemia due to Francisella tularensis tularensis. Dog ticks, Dermacentor variabilis, appear to be critical in the perpetuation of the agent there. Tularemia has long been characterized as an agent of natural focality, stably persisting in characteristic sites of transmission, but this suggestion has never been rigorously tested. Accordingly, we sought to identify a natural focus of transmission of the agent of tularemia by mapping the distribution of PCR-positive ticks. From 2004 to 2007, questing D. variabilis were collected from 85 individual waypoints along a 1.5 km transect in a field site on Martha's Vineyard. The positions of PCR-positive ticks were then mapped using ArcGIS. Cluster analysis identified an area approximately 290 meters in diameter, 9 waypoints, that was significantly more likely to yield PCR-positive ticks (relative risk 3.3, P = 0.001) than the rest of the field site. Genotyping of F. tularensis using variable number tandem repeat (VNTR) analysis on PCR-positive ticks yielded 13 different haplotypes, the vast majority of which was one dominant haplotype. Positive ticks collected in the cluster were 3.4 times (relative risk = 3.4, P<0.0001) more likely to have an uncommon haplotype than those collected elsewhere from the transect. We conclude that we have identified a microfocus where the agent of tularemia stably perpetuates and that this area is where genetic diversity is generated

Gammaherpesvirus-Induced Lung Pathology Is Altered in the Absence of Macrophages

The purpose of this study was to examine the lung pathogenesis of murine gammaherpesvirus (MHV-68) infection in mice that lack CC chemokine receptor CCR2, an important receptor for macrophage recruitment to sites of inflammation. BALB/c and CCR2 −/− mice were inoculated intranasally (i.n.) with MHV-68 and samples were collected during acute infection (6 dpi) and following viral clearance (12 dpi). Immunohistochemistry was used to determine which cells types responded to MHV-68 infection in the lungs. Lung pathology in infected BALB/c mice was characterized by a mixed inflammatory cell infiltrate, necrosis, and increased alveolar macrophages by 12 dpi. Immunohistochemistry showed intense positive staining for macrophages. CCR2 −/− mice showed greater inflammation in the lungs at 12 dpi than did BALB/c mice, with more necrosis and diffuse neutrophil infiltrates in the alveoli. Immunohistochemistry demonstrated much less macrophage infiltration in the CCR2 −/− mice than in the BALB/c mice. These studies show that CCR2 is involved in macrophage recruitment in response to MHV-68 infection and illustrates how impairments in macrophage function affect the normal inflammatory response to this viral infection.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/41345/1/408_2004_Article_2535.pd

An Essential Role for the Proximal but Not the Distal Cytoplasmic Tail of Glycoprotein M in Murid Herpesvirus 4 Infection

Murid herpesvirus-4 (MuHV-4) provides a tractable model with which to define common, conserved features of gamma-herpesvirus biology. The multi-membrane spanning glycoprotein M (gM) is one of only 4 glycoproteins that are essential for MuHV-4 lytic replication. gM binds to gN and is thought to function mainly secondary envelopment and virion egress, for which several predicted trafficking motifs in its C-terminal cytoplasmic tail could be important. We tested the contribution of the gM cytoplasmic tail to MuHV-4 lytic replication by making recombinant viruses with varying C-terminal deletions. Removing an acidic cluster and a distal YXXΦ motif altered the capsid distribution somewhat in infected cells but had little effect on virus replication, either in vitro or in vivo. In contrast, removing a proximal YXXΦ motif as well completely prevented productive replication. gM was still expressed, but unlike its longer forms showed only limited colocalization with co-transfected gN, and in the context of whole virus appeared to support gN expression less well. We conclude that some elements of the gM cytoplasmic tail are dispensible for MuHV-4 replication, but the tail as a whole is not